Intracoronary angiotensin-converting enzyme inhibition improves diastolic function in patients with hypertensive left ventricular hypertrophy.
Intracoronary angiotensin-converting enzyme inhibition improves diastolic function in patients with hypertensive left ventricular hypertrophy.
复制标题
冠状动脉内血管紧张素转换酶抑制可改善高血压左心室肥厚患者的舒张功能。
DOI：
10.1161/01.cir.89.6.2616
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发表时间：
1994
期刊：
影响因子：
37.8
通讯作者：
Feldman,MD
中科院分区：
文献类型：
--
作者：
Haber,HL;Powers,ER;Gimple,LW;Wu,CC;Subbiah,K;Johnson,WH;Feldman,MD
随着左心室肥厚（LVH）的发展，心肌血管紧张素转换酶（ACE）的表达也逐渐被人们所认识。在LVH的存在下，随后血管紧张素I向II转化增加的潜在生理意义尚不清楚，但已被假定为导致异常Ca 2+处理和继发性舒张功能障碍。因此，我们假设，急性血管紧张素转换酶抑制剂将导致减少生产的血管紧张素II和改善主动（钙（2+）依赖性）舒张患者高血压LVH.METHODS和TSANTracoronary（IC）enalaprilat给予25例原发性高血压LVH和不LVH。在稳定状态和下腔静脉闭塞时，通过压力（微压计）-容积（电导）分析确定舒张期和收缩期LV功能指数。患者分为接受高剂量（5.0 mg，n = 15）和低剂量（1.5 mg，n = 10）IC依那普利拉在30分钟内以1 mL/min输注。高剂量患者进一步沿着0.671 cm/m2的标准化左室壁厚度中位数划分。在室壁厚度> 0.671 cm/m2的患者中，接受大剂量依那普利拉的患者的等容舒张时间常数（TauL）在基线时延长（TauL，分别为56 +/- 2与44 +/- 2和45 +/- 2毫秒，通过ANOVA，P < .01），并且仅在该患者组中缩短（TauL，分别为49 +/- 3对46 +/- 2和43 +/- 2毫秒，P < .01对基线和其他组，通过ANOVA）。TauL的改善与LVH的程度成正比（r = 0.92，P <0.001）。尽管左室舒张末期压降低（23 +/- 2至15 +/- 1 mm Hg，P < .01）和体积（86 +/- 8至67 +/- 9 mL/m2，P <0.05）在TauL降低的患者中，这是由于向下移动类似的舒张压-容积关系，而腔室弹性刚度没有变化（0.023 +/- 0.002 ~ 0.025 +/- 0.004 mL-1，P = NS）.结论冠状动脉内应用依那普利拉可改善重度高血压LVH患者的主动（Ca（2+）依赖性）舒张功能。主动舒张功能的改善与LVH的严重程度成正比。这些结果支持了心脏肾素-血管紧张素系统是高血压LVH主动舒张功能的重要决定因素的假设。
BACKGROUNDThere is increasing recognition of myocardial angiotensin-converting enzyme, which is induced with the development of left ventricular hypertrophy (LVH). The potential physiological significance of subsequent increased angiotensin I to II conversion in the presence of LVH is unclear but has been postulated to cause abnormal Ca2+ handling and secondary diastolic dysfunction. Accordingly, we hypothesized that acute angiotensin-converting enzyme inhibition would result in decreased production of angiotensin II and improved active (Ca(2+)-dependent) relaxation in patients with hypertensive LVH.METHODS AND RESULTSIntracoronary (IC) enalaprilat was administered to 25 patients with and without LVH secondary to essential hypertension. Indexes of diastolic and systolic LV function were determined from pressure (micromanometer)-volume (conductance) analysis at steady state and with occlusion of the inferior vena cava. Patients were divided into those receiving high- (5.0 mg, n = 15) and low-dose (1.5 mg, n = 10) IC enalaprilat during a 30-minute infusion at 1 mL/min. The high-dose patients were further divided along the median normalized LV wall thickness of 0.671 cm/m2. The time constant of isovolumic relaxation (TauL) was prolonged at baseline in patients receiving high-dose enalaprilat with wall thickness > 0.671 cm/m2 (TauL, 56 +/- 2 versus 44 +/- 2 and 45 +/- 2 milliseconds, respectively, P < .01 by ANOVA) and shortened only in this patient group (TauL, 49 +/- 3 versus 46 +/- 2 and 43 +/- 2 milliseconds, respectively, P < .01 versus baseline and other groups by ANOVA). The improvement in TauL was directly proportional to the degree of LVH (r = .92, P < .001). Although there was a decrease in LV end-diastolic pressure (23 +/- 2 to 15 +/- 1 mm Hg, P < .01) and volume (86 +/- 8 to 67 +/- 9 mL/m2, P < .05) in those patients with a reduction in TauL, this is due to movement down a similar diastolic pressure-volume relation with no change in chamber elastic stiffness (0.023 +/- 0.002 to 0.025 +/- 0.004 mL-1, P = NS).CONCLUSIONSIntracoronary enalaprilat resulted in an improvement in active (Ca(2+)-dependent) relaxation in those patients with more severe hypertensive LVH. The improvement in active relaxation was directly proportional to the severity of LVH. These results support the hypothesis that the cardiac renin-angiotensin system is an important determinant of active diastolic function in hypertensive LVH.